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Article in Chinese | WPRIM | ID: wpr-878803


In the current study, schisandrin B(SchB)-loaded F127 modified lipid-polymer hybrid nanoparticles(SchB-F-LPNs) were developed to improve the inhibition of breast cancer lung metastasis. Modified nanoprecipitation method was used to prepare SchB-F-LPNs. The nanoparticles were spherical in shape with shell-core structure by TEM observation. SchB-F-LPNs showed a mean particle size of(234.60±6.11) nm with zeta potential of(-5.88±0.49) mV. XRD results indicated that SchB existed in the nanoparticles in an amorphous state. The apparent permeability coefficient through porcine mucus of F-LPNs was 1.43-fold of that of LPNs as shown in the in vitro mucus penetration study. The pharmacokinetics study showed that the C_(max) of SchB was(369.06±146.94) μg·L~(-1),(1 121.34±91.65) μg·L~(-1) and(2 951.91±360.53) μg·L~(-1) respectively in SchB suspensions group, SchB-LPNs group and SchB-F-LPNs group after oral administration in rats. With SchB suspensions as the reference formulation, the relative bioavailability of SchB-F-LPNs was 568.60%. SchB-F-LPNs inhibited the morphological change during transforming growth factor-β1(TGF-β1)-induced epithelial-mesenchymal transition. In addition, SchB-F-LPNs significantly decreased the number of metastatic pulmonary nodules in 4 T1 tumor-bearing mice, suggesting that SchB-F-LPNs may inhibit the metastasis of breast cancer. These results reveal the promising potential of SchB-F-LPNs in treatment of breast cancer lung metastasis.

Animals , Cyclooctanes , Lignans , Lipids , Lung Neoplasms/drug therapy , Mice , Nanoparticles , Polycyclic Compounds , Polyethylenes , Polymers , Polypropylenes , Rats , Swine
Journal of Medical Postgraduates ; (12): 398-403, 2018.
Article in Chinese | WPRIM | ID: wpr-700841


Objective Blood-brain barrier(BBB)may stop over 95%of the drugs delivered from entering the brain.This study aimed to establish a BBB model in vitro,detect the ability of the nano drug delivery system to penetrate the BBB,and observe its effect on angiogenesis and neuron cell proliferation after cerebral infarction. Methods A BBB model was established in vitro and the penetrability of PHRO through the BBB was detected by transwell assay.PBS,Rg1,and PHRO were placed in the upper chamber,and the content of Rg1 in the lower chamber was measured by HPLC.The effect of PHRO on angiogenesis was assessed with the in vitro tube formation model and the expression levels of the angiogenesis -related genes VEGFA and Dll4 determined by real time fluorescence quantitative PCR.Brain endothelial cells were incubated with 10 μL PBS(the control group),10 μmol/L Rg1(the Rg1 group),and PHRO(containing 10 μmol/L Rg1,the PHRO group)for 24 hours,and the SH5Y cells incubated the same way in the three groups for 72 hours.The effects of PHRO on the proliferation and apoptosis of the SH5Y cells were detected by MTT assay and flow cytometry respectively.The SH5Y cells were treated with 10 μL PBS(the PBS con-trol group),1 mmol/L Na2S2O4(the hypoxia-induction group),1 mmol/L Na2S2O4plus 10 μmol/L Rg1(the hypoxia-induction +Rg1 group),and 1 mmol/LNa2S2O4plus PHRO(including10 μmol/L Rg1,the hypoxia-induction +PHRO group), respectively. Results The content of Rg1 was 3.18%in the Rg1 group,28.8%in the PHRO group,and 0 in the control group.The angiogenesis of endothelial cells was markedly increased in the Rg 1 group as compared with the control(P<0.05), and even more significantly in the PHRO than in the Rg1 group(P<0.05).In comparison with the control group,the expressions of VEGFA and Dll 4 and the prolif-eration of the SH5Y cells were remarkably elevated in the Rg 1 group(P<0.05)and even more significantly in the PHRO than in the Rg1 group(P<0.05).The apoptosis rate of neurons was the lowest in PBS control(1.2%)and the highest in the hypoxia-induction group(21.6%),decreased to 13.14%and 8.25%in the hypoxia-induction +Rg1 and hypoxia-induction +PHRO group,respectively. Conclusion PHRO nanomedicine could penetrate the blood-brain barrier in vitro, promote angiogenesis and neuronal proliferation, reduce the apoptosis of neurons under hypoxia,and up-regulate the expressions of angiogenesis-related genes.

Chinese Medical Journal ; (24): 2088-2094, 2017.
Article in English | WPRIM | ID: wpr-338794


<p><b>BACKGROUND</b>Paroxysmal kinesigenic dyskinesia (PKD) is a rare movement disorder characterized by recurrent dystonic or choreoathetoid attacks triggered by sudden voluntary movements. Under the condition of psychological burden, some patients' attacks may get worsened with longer duration and higher frequency. This study aimed to assess nonmotor symptoms and quality of life of patients with PKD in a large population.</p><p><b>METHODS</b>We performed a cross-sectional survey in 165 primary PKD patients from August 2008 to October 2016 in Rui Jin Hospital, using Symptom Check List-90-Revised (SCL-90-R), World Health Organization Quality of Life-100 (WHOQoL-100), Self-Rating Depression Scale, and Self-Rating Anxiety Scale. We evaluated the differences of SCL-90-R and WHOQOL-100 scores in patients and Chinese normative data (taken from literature) by using the unpaired Student's t-test. We applied multivariate linear regression to analyze the relationships between motor manifestations, mental health, and quality of life among PKD patients.</p><p><b>RESULTS</b>Compared with Chinese normative data taken from literature, patients with PKD exhibited significantly higher (worse) scores across all SCL-90-R subscales (somatization, obsessive-compulsive, interpersonal sensitivity, depression, anxiety, hostility, phobic anxiety, paranoid ideation, and psychoticism; P= 0.000 for all) and significantly lower (worse) scores of five domains in WHOQoL-100 (physical domain, psychological domain, independence domain, social relationship domain, and general quality of life; P= 0.000 for all). Nonremission of dyskinesia episodes (P = 0.011) and higher depression score (P = 0.000) were significantly associated with lower levels of quality of life. The rates of depression and anxiety in patients with PKD were 41.2% (68/165) and 26.7% (44/165), respectively.</p><p><b>CONCLUSIONS</b>Depression, anxiety, and low levels of quality of life were prevalent in patients with PKD. Co-occurrence of depression and anxiety was common among these patients. Regular mental health interventions could set depression and anxiety as intervention targets. Considering that the motor episodes could be elicited by voluntary movements and sometimes also by emotional stress, and that symptoms may get worsened with longer duration and higher frequency when patients are stressed out, intervention or treatment of depression and anxiety might improve the motor symptoms and overall quality of life in PKD patients.</p>

Article in English | WPRIM | ID: wpr-819899


OBJECTIVE@#To study the mechanism of insulin resistance in the cholesterol gallstone formation from insulin signal transduction pathway so as to reveal the possible mechanism and the effective role of Albiflorin Granule on preventing the cholesterol gallstones.@*METHODS@#Serum triglycerides (TG), free fatty acid (FFA), and total cholesterol (TC) from different groups were measured and liver cells InsR, PKB, IKK-β protein expression levels were detected by western blotting.@*RESULTS@#Albiflorin significantly decreased the cholesterol gallstone formation rate, increased glucose infusion rate in gallstone guinea pigs and improved insulin resistance. Compared with the normal group, insulin receptor and PKB protein expression in GS group were significantly reduced. IKK-β protein in the GS group increased significantly and Albiflorin could reduce IKK-β protein expression in guinea pig liver cells.@*CONCLUSIONS@#The model of insulin resistance in cholesterol gallstone guinea pig was successfully established, which plays an important role in the cholesterol gallstone formation. All aspects of insulin signaling pathway are involved in gallstone formation. Albiflorin can regulate various aspects of insulin signal transduction pathway to prevent the formation of gallbladder.

Article in English | WPRIM | ID: wpr-819886


OBJECTIVE@#To study the effect of emodin on protein and gene expressions of the massagers in mobility signal transduction system of cholecyst smooth muscle cells in guinea pig with cholesterol calculus.@*METHODS@#The guinea pigs were randomly divided into 4 groups, such as control group, gall-stone (GS) group, emodin group and ursodeoxycholic acid (UA) group. Cholesterol calculus models were induced in guinea pigs of GS, emodin and UA groups by lithogenic diet, while emodin or UA were given to the corresponding group for 7 weeks. The histomorphological and ultrastructure change of gallbladder were detected by microscope and electron microscope, the content of plasma cholecystokinin (CCK) and [Ca] were analyzed successively by radioimmunoassay and flow cytometry. The protein and mRNA of Gsα, Giα and Cap in cholecyst cells were determined by western blotting and real time polymerase chain reaction (RT-PCR).@*RESULTS@#Emodin or UA can relieve pathogenic changes in epithelial cells and muscle cells in gallbladder of guinea pig with cholesterol calculus by microscope and transmission electron microscope. In the cholecyst cells of GS group, CCK levels in plasma and [Ca] decreased, the protein and mRNA of GS were down-regulated, the protein and mRNA of Gi and Cap were up-regulated. Emodin significantly decreased the formative rate of gallstone, improved the pathogenic change in epithelial cells and muscle cells, increased CCK levels in plasma and [Ca] in cholecyst cells, enhanced the protein and mRNA of Gs in cholecyst cells, reduced the protein and mRNA of Gi and Cap in cholecyst cells in guinea pig with cholesterol calculus.@*CONCLUSION@#The dysfunction of gallbladder contraction gives rise to the disorders of mobility signal transduction system in cholecyst smooth muscle cells, including low content of plasma CCK and [Ca] in cholecyst cells, abnormal protein and mRNA of Gs, Gi and Cap. Emodin can enhance the contractibility of gallbladder and alleviate cholestasis by regulating plasma CCK levels, [Ca] in cholecyst cells and the protein and mRNA of Gs, Gi and Cap.